Benzidine and 4-aminobiphenyl (4-ABP) are activated by intact plant cells and cell free TX1MX into mutagenic metabolites that induce frameshift and base pair substitution mutations in Salmonella typhimurium. The plant activation of these agents is plant peroxidase-mediated and bacterial O-acetyltran
Plant-activation of the bicyclic aromatic amines benzidine and 4-aminobiphenyl
β Scribed by Young H. Ju; Michael J. Plewa
- Publisher
- John Wiley and Sons
- Year
- 1997
- Tongue
- English
- Weight
- 217 KB
- Volume
- 29
- Category
- Article
- ISSN
- 0893-6692
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β¦ Synopsis
Benzidine and 4-aminobiphenyl (4-ABP) are promutagenic bicyclic aromatic amines that are activated into frameshift and base pair substitution mutagens by plant systems. Using the plant cell/microbe coincubation assay, plant-activated benzidine from 0 to 50 microM induced a concentration-response in Salmonella typhimurium. At concentrations above 5 microM, plant-activated benzidine induced frameshift and base pair substitution mutations in the N- or O-acetyltransferase over-expressing strains, DJ460, YG1024, and YG1029. With plant-activated 4-ABP, concentrations above 250 microM induced a significant mutagenic response in strains YG1024 and YG1029. A tobacco cell-free mixture, TX1MX, activated benzidine and 4-ABP into mutagenic metabolites in S. typhimurium strains YG1024, YG1029, and DJ460. The mutagenic sensitivities of plant-activated benzidine and 4-ABP were the same with two different types of plant activation systems, TX1 suspension cells and TX1MX cell-free medium. The plant activation of these aromatic amines is mediated by tobacco cell peroxidase. Plant-activated benzidine and 4-ABP are converted into intermediates that serve as substrates for bacterial or humanacetylCoA: N-hydroxyarylamine N-acetyltransferase to generate the ultimate mutagenic products.
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## Abstract Metabolites of the human carcinogen 4βaminobiphenyl (4βABP) form hemoglobin (Hb) adducts, which represent a useful biomarker for exposure. However, not every individual responds to a similar degree to 4βABP exposure, and variations in 4βABPβHb adduct formation might be explained by gene